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@ARTICLE{Weigand:132949,
      author       = {T. Weigand and B. Singler and T. Fleming and P. Nawroth and
                      K. Klika$^*$ and C. Thiel and H. Baelde and S. F. Garbade
                      and A. H. Wagner and M. Hecker and B. A. Yard and A.
                      Amberger and J. Zschocke and C. P. Schmitt and V. Peters},
      title        = {{C}arnosine {C}atalyzes the {F}ormation of the
                      {O}ligo/{P}olymeric {P}roducts of {M}ethylglyoxal.},
      journal      = {Cellular physiology and biochemistry},
      volume       = {46},
      number       = {2},
      issn         = {1421-9778},
      address      = {Basel},
      publisher    = {Karger},
      reportid     = {DKFZ-2018-00588},
      pages        = {713 - 726},
      year         = {2018},
      abstract     = {Reactive dicarbonyl compounds, such as methylglyoxal (MG),
                      contribute to diabetic complications. MG-scavenging
                      capacities of carnosine and anserine, which have been shown
                      to mitigate diabetic nephropathy, were evaluated in vitro
                      and in vivo.MG-induced cell toxicity was characterized by
                      MTT and MG-H1-formation, scavenging abilities by Western
                      Blot and NMR spectroscopies, cellular carnosine transport by
                      qPCR and microplate luminescence and carnosine concentration
                      by HPLC.In vitro, carnosine and anserine dose-dependently
                      reduced N-carboxyethyl lysine (CEL) and advanced glycation
                      end products (AGEs) formation. NMR studies revealed the
                      formation of oligo/polymeric products of MG catalyzed by
                      carnosine or anserine. MG toxicity (0.3-1 mM) was
                      dose-dependent for podocytes, tubular and mesangial cells
                      whereas low MG levels (0.2 mM) resulted in increased cell
                      viability in podocytes $(143±13\%,$ p<0.001) and tubular
                      cells $(129±3\%,$ p<0.001). Incubation with
                      carnosine/anserine did not reduce MG-induced toxicity,
                      independent of incubation times and across large ranges of
                      MG to carnosine/anserine ratios. Cellular carnosine uptake
                      was low $(<0.1\%$ in 20 hours) and cellular carnosine
                      concentrations remained unaffected. The putative carnosine
                      transporter PHT1 along with the taurine transporter (TauT)
                      was expressed in all cell types while PEPT1, PEPT2 and PHT2,
                      also belonging to the proton-coupled oligopeptide
                      transporter (POT) family, were only expressed in tubular
                      cells.While carnosine and anserine catalyze the formation of
                      MG oligo/polymers, the molar ratios required for protection
                      from MG-induced cellular toxicity are not achievable in
                      renal cells. The effect of carnosine in vivo, to mitigate
                      diabetic nephropathy may therefore be independent upon its
                      ability to scavenge MG and/or carnosine is mainly acting
                      extracellularly.},
      cin          = {G404},
      ddc          = {540},
      cid          = {I:(DE-He78)G404-20160331},
      pnm          = {317 - Translational cancer research (POF3-317)},
      pid          = {G:(DE-HGF)POF3-317},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29621776},
      doi          = {10.1159/000488727},
      url          = {https://inrepo02.dkfz.de/record/132949},
}